Neurological Research Journal Impact Factor & Information

Publisher: Maney Publishing

Journal description

Neurological Research is an international peer-reviewed journal publishing original and fundamental studies as well as clinical research in areas of neurology, neurosurgery and neurosciences, together with such subspecialty areas as: neuro-oncology, neuropsychiatry, neurotraumatology, neuroradiology, neuropathology and molecular biology. Each issue comprises articles of clinical significance and scientific excellence with original research, case reports, and broad-based review articles, with rapid publication turnaround.

Current impact factor: 1.44

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 1.439
2013 Impact Factor 1.449
2012 Impact Factor 1.182
2011 Impact Factor 1.522
2010 Impact Factor 1.621
2009 Impact Factor 1.277
2008 Impact Factor 1.634
2007 Impact Factor 1.634
2006 Impact Factor 1.573
2005 Impact Factor 1.638
2004 Impact Factor 1.216
2003 Impact Factor 1.026
2002 Impact Factor 0.969
2001 Impact Factor 1.176
2000 Impact Factor 0.866
1999 Impact Factor 1.1
1998 Impact Factor 1.128
1997 Impact Factor 1.027
1996 Impact Factor 1.142
1995 Impact Factor 0.852
1994 Impact Factor 0.697

Impact factor over time

Impact factor

Additional details

5-year impact 1.48
Cited half-life 8.10
Immediacy index 0.24
Eigenfactor 0.01
Article influence 0.40
Website Neurological Research website
Other titles Neurological research
ISSN 0161-6412
OCLC 3983345
Material type Periodical
Document type Journal / Magazine / Newspaper

Publisher details

Maney Publishing

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo for STEM (science, technology, engineering and medicine) journals
    • 2 years embargo for HSS (humanities and social science) journals
  • Conditions
    • Authors' pre-print on author's personal website or institutional website, or institutional repository, or subject-based repository
    • Author's post-print on institutional repository or subject-based repository
    • Must link to publisher version with DOI
    • Publisher copyright and source must be acknowledged with citation
    • On a non-profit server
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Objectives: To study whether Clopidogrel–Aspirin combined treatment for high risk transient ischaemic attack (TIA) or minor stroke results in increased number of lesions associated with anti-thrombotic cerebral haemorrhage or cerebral micro-bleeds (CMB) than aspirin alone treatment. Methods: The patients recruited in CHANCE test in our hospital participated in this study. We made a comparison between treatments Aspirin–Clopidogrel combined group and the Aspirin alone group in the numbers of CMB and subsequent cerebral haemorrhages. In addition, we analysed the association between the increased numbers of CMB and subsequent intracerebral haemorrhages. All 129 patients with high risk TIA with microbleeds or minor stroke within 24 hours after the onset (average age 65.9±9.3, 48.7% were male patients) were divided randomly into two groups: (1) 67 patients were given combination therapy with clopidogrel and aspirin (clopidogrel at an initial dose of 300 mg, then 75 mg per day for 90 days, plus aspirin at a dose of 75 mg per day for the first 21 days);(2) the rest patients were given aspirin treatment (75 mg per day for 90 days). All participants received open-label aspirin at a clinician-determined dose of 75–300 mg on the first day. Results: The CMB were found in 52.7% of all patients in both groups. There was no siginificant difference between the Aspirin group and the Aspirin–clopidogrel treated group, though the latter showed some slight increase in CMB (Odds ratios (OR) = 1.16, 95% confidence intervals (CI) = 0.54–2.47, P = 0.71). But the numbers of CMB were remarkably associated with the number of primary existing CMB (OR = 6.46, 95%CI 2.57–16.23, P<0.001), especially that of primary existing CMB ≥ 3.In addition, the increasing numbers of CMB associated with primary CMB lesions, which located in corticosubcortical area (CSC) (OR = 4.69, 95%CI 1.51–14.53, P = 0.007). Conclusions: For the treatment of high-risk TIA or minor stroke patients, the clopidogrel–aspirin treatment did not increase the number of CMB than Aspirin alone. It appears that the extent of CMB was associated with the extent of existing CMB occurred in previous stroke, which was mostly located in cortical, subcortical zone.
    Neurological Research 08/2015; 37(11):1743132815Y.000. DOI:10.1179/1743132815Y.0000000087
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    ABSTRACT: Objective: Cerebral hyperperfusion syndrome (HPS) is a potential complication of extracranial-intracranial (EC-IC) bypass for moyamoya disease; however, the pathological threshold of the early cerebral blood flow (CBF) increases after EC-IC bypass has yet to be determined. The purpose of this study is to evaluate the predictive and diagnostic values of early quantitative CBF analysis for the detection of HPS after EC-IC bypass for moyamoya disease. Methods: We quantitatively evaluated regional CBF at the site of the anastomosis in 23 patients with moyamoya disease aged between 18 and 66 years (mean, 39.6) before and 1 day after superficial temporal artery-middle cerebral artery anastomosis by an auto-radiographic method using N-isopropyl-p-[(123)I]iodoamphetamine single-photon emission computed tomography. Results: Regional CBF 1 day after surgery was significantly higher in patients with HPS (n = 5; mean, 54.6 ml/100 g/minutes) than in patients without HPS (n = 18; mean, 40.5 ml/100 g/minutes) (P = 0.038). The postoperative/preoperative CBF ratio was significantly higher in patients with HPS (1.84) than in patients without HPS (1.34) (P = 0.044). Multivariate analyses showed that the regional CBF value 1 day after surgery (P = 0.036) and operating on the left hemisphere (P = 0.026) significantly correlated with HPS. All patients with HPS developed symptoms and/or intracerebral hemorrhage more than 2 days after EC-IC bypass. Receiver operating characteristic analysis indicated that the cutoff value of pathological postoperative CBF increase was 46.1 ml/100 g/minutes (sensitivity = 80%, specificity = 77.8%, AUC value = 0.81). Conclusion: Quantitative analysis of early postoperative CBF is useful for predicting and diagnosing HPS after revascularization surgery for moyamoya disease.
    Neurological Research 08/2014; 37(2):1743132814Y0000000432. DOI:10.1179/1743132814Y.0000000432
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    ABSTRACT: Although neurovascular confliction was believed to be the cause of hemifacial spasm (HFS), the mechanism of the disorder remains unclear to date. Current theories, merely focusing on the facial nerve, have failed to explain the clinical phenomenon of immediate relief following a successful microvascular decompression surgery (MVD). With the experience of thousands of microvascular decompression surgeries and preliminary investigations, we have learned that the offending artery may play a more important role than the effect of merely mechanical compression in the pathogenesis of the disease. We believe that the attrition of neurovascular interface is the essence of the etiology, and the substance of the disease is emersion of ectopic action potentials from the demyelinated facial nerve fibers, which were triggered by the sympathetic endings from the offending artery wall. In this paper, we put forward evidence to support this hypothesis, both logically and theoretically.
    Neurological Research 07/2014; 37(2):1743132814Y0000000424. DOI:10.1179/1743132814Y.0000000424
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    ABSTRACT: Background: Alzheimer's disease (AD) is one of the most common dementia, which is not effectively cured to date. Amyloid-beta (Abeta) deposition cascade and disintegrity of brain extracellular matrix (ECM) scaffold attribute to the progress of AD. Thus, it maybe an effective way to treat AD by altering the processing of amyloid precursor protein (APP) and regaining the integrity of ECM. The peptide amphiphile (PA) with a laminin epitope isoleucine-lysine-valine-alanine-valine (IKVAV) (IKVAV-PA) can be trigged into ECM in vivo. In addition, IKVAV-PA could significantly improve cognitive impairment with remarkable increase of endoneurogensis in the hippocampus, as well as reduction of burden of amyloid plaque in the brain. Methods: We used heterozygous AbetaPPswe/PS1dE9 double transgenic mice as the animal model of AD. After 1 week of initial stereotaxic administration into bilateral hippocampus, the mice were subjected to the Morris Water Maze (MWM) test. At the end of MWM test, immunohistochemical staining, Western blot and real-time polymerase chain reaction (PCR) were performed in mice. Results: Here we showed that IKVAV-PA significantly improved cognitive impairment accompanying with reducing the burden of Abeta plaques, as well as the levels of soluble Abeta1-40 and Abeta1-42 in the cortex and hippocampus after 2 weeks of initial administration into bilateral hippocampus. Further examination demonstrated that IKVAV-PA also altered the processing of APP via inhibiting the gene expression of beta-secretase (BACE1), as well as improving the gene expression of insulin-degrading enzyme (IDE) and neprilysin (NEP). Conclusion: Our data suggest that IKVAV-PA may serve as an alternative therapeutic intervention for treating the learning and memory losses in AD.
    Neurological Research 07/2014; 37(1):1743132814Y0000000417. DOI:10.1179/1743132814Y.0000000417
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    ABSTRACT: Objective: To determine if a computer-based simulation with haptic technology can help surgical trainees improve tactile discrimination using surgical instruments. Material and methods: Twenty junior medical students participated in the study and were randomized into two groups. Subjects in Group A participated in virtual simulation training using the ImmersiveTouch simulator (ImmersiveTouch, Inc., Chicago, IL, USA) that required differentiating the firmness of virtual spheres using tactile and kinesthetic sensation via haptic technology. Subjects in Group B did not undergo any training. With their visual fields obscured, subjects in both groups were then evaluated on their ability to use the suction and bipolar instruments to find six elastothane objects with areas ranging from 1.5 to 3.5 cm2 embedded in a urethane foam brain cavity model while relying on tactile and kinesthetic sensation only. Results: A total of 73.3% of the subjects in Group A (simulation training) were able to find the brain cavity objects in comparison to 53.3% of the subjects in Group B (no training) (P = 0.0183). There was a statistically significant difference in the total number of Group A subjects able to find smaller brain cavity objects (size ≤ 2.5 cm2) compared to that in Group B (72.5 vs. 40%, P = 0.0032). On the other hand, no significant difference in the number of subjects able to detect larger objects (size ≧ 3 cm2) was found between Groups A and B (75 vs. 80%, P = 0.7747). Conclusion: Virtual computer-based simulators with integrated haptic technology may improve tactile discrimination required for microsurgical technique.
    Neurological Research 07/2014; 36(12):1743132814Y0000000405. DOI:10.1179/1743132814Y.0000000405
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    ABSTRACT: Objectives: Postconditioning with sevoflurane has been shown to protect against focal cerebral ischemia and reperfusion injury. However, the mechanism remains elusive. In this study, we tested the hypothesis that mitochondrial ATP-sensitive potassium (mitoKATP) and mitochondrial permeability transition pore (mPTP) play roles in the neuroprotection of postconditioning with sevoflurane. Methods: Adult male Sprague-Dawley rats were subjected to MCAO for 90 minutes and then treated with sevoflurane at the beginning of reperfusion. The infarct volume, neurological deficit score, and brain edema were evaluated at 24 hours. Apoptosis were studied by TUNEL. The neuroprotective effect with or without 5-hydroxydecanoate (5-HD), a selective mitoKATP channel blocker or atractyloside (ATR), and an mPTP opener were analyzed. Results: Postconditioning with sevoflurane significantly decreased neurological deficit scores, infarct volume, and brain edema and also reduced apoptotic cells. 5-HD and ATR abolished the neuroprotective effect, respectively. 5-HD or ATR alone had no effect on ischemia and reperfusion injury. Discussion: Our data suggest that mitoKATP and mPTP play crucial roles in the neuroprotection of postconditioning with sevoflurane.
    Neurological Research 06/2014; 37(1):1743132814Y0000000410. DOI:10.1179/1743132814Y.0000000410
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    ABSTRACT: Objectives: Restenosis or neointimal hyperplasia remains an important complication after carotid artery stenting (CAS) for carotid artery stenosis. The purpose of this study was to examine if an anti-hypertensive drug, angiotensin receptor blocker (ARB), prevents post-CAS neointimal hyperplasia during the first 1-year period after CAS, and to clarify the possible mechanisms. Methods: Hypertension had been treated with a calcium channel blocker (CCB) and/or an ARB, valsartan, by the preference of the neurosurgeon in charge in our department. At admission to perform CAS, patients were assigned to normotensive, valsartan (hypertensive patients treated with valsartan with/without any kind of CCBs), and non-valsartan (hypertensive patients treated with any kind of CCBs without ARBs) groups. Post-CAS neointimal hyperplasia was evaluated by carotid duplex ultrasound imaging in terms of intima-media thickening (IMT), which was performed at pre-CAS and at 90, 180, 270, and 360 days post-CAS. Biomarkers of oxidative stress (8-hydroxy-2'-deoxyguanosine), inflammation (C-reactive protein, tenascin-C) and endothelial cell injury (von Willebrand factor [vWF] antigen) were measured at pre-CAS and at 1, 7, and 180 days post-CAS. Results: The non-valsartan group (n = 8) had a higher incidence of maximum in-stent IMT ≧ 1.1 mm compared with the normotensive group (n = 6). Valsartan (n = 9) significantly suppressed plasma vWF levels at 7 days post-CAS and decreased the incidence of maximum in-stent IMT ≧ 1.1 mm compared with the non-valsartan group, although clinical parameters were similar between the two groups. Other biomarkers were not significantly different among the three groups. Conclusions: These findings suggest that valsartan may prevent post-CAS neointimal hyperplasia possibly by suppressing endothelial cell injury.
    Neurological Research 06/2014; 37(1):1743132814Y0000000408. DOI:10.1179/1743132814Y.0000000408
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    ABSTRACT: Transplanted human umbilical cord mesenchymal stem cells (hUC-MSCs) have exhibited considerable therapeutic potential for traumatic brain injury (TBI). However, how hUC-MSCs migrating to the injury region and the mechanism of hUC-MSCs promoting functional recovery after TBI are still unclear. In this study, we investigated whether stromal cell-derived factor-1 (SDF-1) was involved in the hUC-MSCs migration and the possible mechanisms that might be involved in the beneficial effect on functional recovery. In vitro experiments demonstrated that SDF-1 induces a concentration-dependent migration of hUC-MSCs. Furthermore, pre-treatment with the CXCR4-specific antagonist AMD3100 significantly prevented the migration of hUC-MSCs in vitro. We found that the expression of SDF-1 increased significantly around the damaged area. Transplanted hUC-MSCs were localized to regions where SDF-1 was highly expressed. Additionally, our results showed that hUC-MSCs-treated animals showed significantly improved functional recovery compared with controls. In hUC-MSCs-transplanted group, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells were decreased and BrdU-positive cells were significantly increased compared with control group, more of BrdU-positive cells co-localized with GFAP. These suggest that SDF-1 plays an important role in the migration of hUC-MSCs to the damaged area and hUC-MSCs are beneficial for functional recovery after TBI.
    Neurological Research 06/2014; 37(1):1743132814Y0000000399. DOI:10.1179/1743132814Y.0000000399
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    ABSTRACT: The aim of this study is to investigate the effect of microtubule depolymerization by colchicine on hyperalgesia mediated by transient receptor potential vanilloid 4 (TRPV4) in a neuropathic pain model of chronic compression of the dorsal root ganglion (DRG) (hereafter termed CCD) in rat. Intrathecal administration of microtubule-depolymerizing agent, colchicine, attenuated the activated effect of 4alpha-phorbol 12, 13-didecanoate (4alpha-PDD, TRPV4 specific agonist) on mechanical and thermal hyperalgesia in CCD rats. This observation is in agreement with our in vitro experiments with DRG cells that showed a significant attenuation of 4alpha-PDD-activated Ca 2z -influx and substance P (SP) release with the colchicine treatment. We conclude that microtubule depolymerization by colchicine can regulate pain sensitivity by depressing the hyperalgesia mediated by TRPV4.
    Neurological Research 01/2014; 36(1):70-78. DOI:10.1179/1743132813Y.0000000261
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    ABSTRACT: Objectives: NF-E2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway plays anti-apoptotic role in normal tissue and tumor. But the role of Nrf2 in apoptosis in glioma is still unknown. Here, we established this experiment to elucidate how Nrf2-ARE pathway participates in apoptosis in human glioblastoma cell U251. Methods: Two plasmids, pEGFP-Nrf2 and Si-Nrf2, were transfected to up- or downregulate the expression of Nrf2 in U251. After transfection, the apoptosis rate, expression of heme oxygenase-1 (HO-1), Bcl-2, Bax, caspases 3, 9 and activity of caspases 3, 9 were detected. Results: After increasing expression of Nrf2, the apoptosis rate was reduced accompanied with upregulated expression of HO-1, Bcl-2/Bax, decreased expression and activity of caspases 3, 9. After decreasing expression of Nrf2, the apoptosis rate was enhanced accompanied with downregulated expression of HO-1, Bcl-2/Bax, increased expression and activity of caspases 3, 9. Discussion: Our findings suggest that Nrf2 participates in the regulation of apoptosis in U251 through HO-1 and the 'intrinsic' apoptotic pathway.
    Neurological Research 01/2013; 35(1):71-78. DOI:10.1179/1743132812Y.0000000094
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    ABSTRACT: Background: It is a common belief that neurosurgical interventions can cause inevitable damage resulting from the procedure itself in surgery especially for intramedullary spinal cord tumors. The present study was designed to examine if hyperbaric oxygen preconditioning (HBO-PC) was neuroprotective against surgical injuries using a rat model of spinal cord injury (SCI). Methods: Sprague-Dawley rats were randomly divided into three groups: HBO-PC group, hypobaric hypoxic preconditioning (HH-PC) control group, and normobaric control group. All groups were subjected to SCI by weight drop device. Rats from each group were examined for neurological behavior and electrophysiological function. Tissue sections were analyzed by using immunohistochemistry, TdT-mediated dUTP-biotin nick end labeling, and axonal tract tracing. Results: Significant neurological deficits were observed after SCI and HBO-PC and HH-PC improved neurological deficits 1 week post-injury. The latencies of motor-evoked potential and somatosensory-evoked potential were significantly delayed after SCI, which was attenuated by HBO-PC and HH-PC. Compared with normobaric control group, pretreatment with HBO and hypobaric hypoxia significantly reduced the number of TdT-mediated dUTP-biotin nick end labeling-positive cells, and increased nestin-positive cells. HBO-PC and HH-PC enhanced axonal growth after SCI. Conclusions: In conclusion, preconditioning with HBO and hypobaric hypoxia can facilitate functional recovery and suppress cell apoptosis after SCI and may prove to be a useful preventive strategy to neurosurgical SCI.
    Neurological Research 12/2012; 34(10):944-951. DOI:10.1179/1743132812Y.0000000096
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    ABSTRACT: Objectives: The present study was designed to determine whether or not the caspase-independent apoptotic pathway participated in the cellular death of spiral ganglion neurons (SGNs) after exposure to peroxynitrite (ONOO(-)), with particular attention given to the intranuclear translocation of mitochondrial apoptosis-inducing factor (AIF) and endonuclease G (Endo G) in this process. Methods: The rat SGNs were isolated and primary cultured in vitro and were exposed to ONOO(-) with pre-treatment of pan-caspase inhibitor. Morphological changes of SGNs were observed by acridine orange cytochemistry staining, and apoptosis was examined by flow cytometry. The translocation of mitochondrial AIF and Endo G was detected by immunocytochemistry and Western blot. The protein expressions of Bcl-2 family in SGNs exposed to ONOO(-) were determined by Western blot. Results: Treatment of SGNs with ONOO(-) resulted in the occurrence of caspase-independent apoptosis as evidenced by acridine orange staining and flow cytometry analysis. The immunocytochemical analysis showed that AIF and Endo G labeling were marked in neuronal nuclei, while the Western blot demonstrated the intranuclear localization of AIF and Endo G in SGNs treated with ONOO(-). Western blot analysis demonstrated that ONOO(-) increased the Bax expression while reducing Bcl-2 expression, which was not prevented by pre-treatment with caspase inhibitor. Conclusion: These data indicate that ONOO(-) can trigger caspase-independent apoptosis in SGNs associated with mitochondrial AIF and Endo G intranuclear localization.
    Neurological Research 12/2012; 34(10):915-922. DOI:10.1179/1743132812Y.0000000098
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    ABSTRACT: Objective: We investigated whether a correlation exists between insulin resistance and the severity of cerebral white matter lesions among non-diabetic patients with ischemic stroke. Methods: The subjects were 105 consecutive patients without diabetes who were hospitalized due to non-cardioembolic stroke. The insulin resistance was evaluated by a homeostasis model assessment of insulin resistance (HOMA-IR). The degrees of periventricular hyperintensity (PVH) and deep and subcortical white matter hyperintensity (DSWMH) were evaluated by the brain MRI. The HOMA-IR values ≥2·5 were indicative of the insulin resistance. Results: The presence of PVH and DSWMH were 86·7 and 83·8%, respectively. The ratio of insulin resistance increased with higher grades of PVH and DSWMH. The HOMA-IR level in grade 3 PVH was significantly higher than those in grades 0 and 1. The HOMA-IR level in grade 3 DSWMH was significantly higher than those in grades 0-2. Multiple linear regression analysis showed that HOMA-IR was significantly associated with PVH or DSWMH. Conclusion: It was found that insulin resistance correlated with white matter lesions among non-diabetic patients with non-cardiogenic ischemic stroke.
    Neurological Research 08/2010; 32(7):743-747. DOI:10.1179/016164109X12608733393755